Evidence map›Paper›PMID 22434583›Full record

ArticleClinical & experimental metastasis2012

Elastin-derived peptides increase invasive capacities of lung cancer cells by post-transcriptional regulation of MMP-2 and uPA.

Simon Toupance, Bertrand Brassart, Fanja Rabenoelina, Christelle Ghoneim, Laurent Vallar, Myriam Polette, Laurent Debelle, Philippe Birembaut

Abstract read
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In one paragraph

Article in Clinical & experimental metastasis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.3field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

38 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
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  6. Review
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  8. Article
  9. Epigenetic regulation and targeting of ECM for cancer therapy.American journal of physiology. Cell physiology · 2022
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  15. Article
  16. TRPM7/RPSA Complex Regulates Pancreatic Cancer Cell Migration.Frontiers in cell and developmental biology · 2020
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

Simon ToupanceINSERM, UMRS 903, IFR53, Université de Reims Champagne-Ardenne, Reims, France.
Bertrand Brassart
Fanja Rabenoelina
Christelle Ghoneim
Laurent Vallar
Myriam Polette
Laurent Debelle
Philippe Birembaut
Université de Reims Champagne-Ardenne · FRLaboratoire National de Santé · LUCentre Hospitalier Universitaire de Reims · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Elastin-rich lung extracellular matrix is largely remodeled during tumor invasion. Elastin degradation produces peptides displaying a wide range of biological activities. These elastin derived peptides (EP) interact with the elastin receptor complex (ERC) but also bind to α(V)β(3) integrin and galectin-3. In this study, we explored the role of EP and their receptors in tumor progression of lung carcinomas. Non-invasive and invasive lung tumor cell lines were incubated in presence of kappa-elastin (κE) or with synthetic peptides displaying receptor-specific sequences (VGVAPG, GRKRK, AGVPGLGVG and AGVPGFGAG). Modified Boyden chamber assays revealed an increased invasive capacity of invasive cells induced by κE. EP treatment had no effect on cell proliferation but zymography analysis revealed an increase of pro-MMP-2 and uPA levels in the conditioned media of treated cells. Moreover, the active form of MMP-2 was increased in invasive cells. Interestingly, this regulation was not observed at the mRNA level and actinomycin D was unable to inhibit κE effects. We also observed that the regulation of proteases protein level following κE treatment was an early process detectable after 1 h. All these effects could not be inhibited by lactose and V14, two ERC antagonists, or by blocking antibodies against α(V)β(3) integrin and galectin-3. Finally, VGVAPG and GRKRK failed to reproduce κE effects whereas nonapeptides partially mimicked them. These results demonstrate that treatment with EP up-regulates invasiveness of lung tumor cells via the release of proteolytic enzymes. This modulation involves post-transcriptional mechanisms and a nonapeptide-receptor different from the ERC, α(V)β(3) integrin and galectin-3.

Indexed as

Cell MovementAdenocarcinomaBiomarkers, TumorBlotting, WesternCell ProliferationElastinExtracellular MatrixGalectin 3Gene Expression ProfilingHumansIntegrin alphaVbeta3Lung NeoplasmsMatrix Metalloproteinase 2Oligonucleotide Array Sequence AnalysisOligopeptidesReal-Time Polymerase Chain ReactionBiomarkers, TumorElastinGalectin 3Integrin alphaVbeta3Matrix Metalloproteinase 2OligopeptidesRNA, MessengerUrokinase-Type Plasminogen Activator

Identifiers

PMID22434583
OpenAlexW2074918050

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.